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Protected β-cell Function In A Obese Type 2 Diabetic Rat Model With A KATP Channel Opener

Posted on:2007-09-27Degree:MasterType:Thesis
Country:ChinaCandidate:J LiFull Text:PDF
GTID:2144360182491610Subject:Endocrinology and metabolism
Abstract/Summary:PDF Full Text Request
Objective: Comparion with Katp channel closure, treatment with KAtp channel opener leads to protect β-cell function by inhibition of insulin secretion and β-cell rest. Method: Six-week-age male SD rats are fed with nomoral high-fat diet (HFD). After eight weeks of dietary manipulation, these rats are injected low dose streptozotocin(STZ)(30mg/Kg). Diazoxide (30mg/ kg) and glipizide (5mg/ kg) are administered to the rat model respectively. The metabolism characteristics are measured and pancreatic histopathology is analyzed among each group. Result: The HFD-fed rats exhibit significant increase in body weigh(P<0.05) and insulin resistant ratio (HOMA-IR) (P<0.05). Islet size and its cell mass are preserves well in DZ-rat by diazoxide treatment. The frequence of pancreatic β-cell apoptosis decrease in DZ-rat by diazoxide treatment. Conclusion: Katp channel openers can protect 6-cell from both functionally and morphologically by suppression of excessive insulinsecretion. Therefore, the concept of beta-cell rest may provide a strategy to protect 6-cell and prevent diabetes.
Keywords/Search Tags:rat model, Type 2 diabetes, Glucotoxicity, Lipotoxicity, Katp Channel opener, β-cell rest
PDF Full Text Request
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